Table 2.
Main biomarkers in Alzheimer’s disease, biological processes, molecules, and organelles to be further studied as possible biomarkers.
AD Biomarkers and Processes | Human Blood | Human CSF | Other Human Tissue/Technique |
Additional Data from Mouse Model |
---|---|---|---|---|
Amyloid-β | ↓ [14] |
↑ brain tissue postmortem (neuritic plaques) [15] ↑ PET [10] |
||
Tau protein | ↑ [14] |
↑ brain tissue postmortem (neurofibrillary tangles) [15] |
||
Neurogranin | ↓ * [16] |
↑ [17] |
↓ brain tissue postmortem [18] |
|
Neurofilament | ↑ [19] |
|||
Neuroinflammation TGF-β Microglia activation |
↑ [20] | ↑ PET [21] |
||
Peripheral inflammation Leptin IL-1r agonist IL-6 IL-18 TGF-β TNF-α |
↓ ↓ ↑ ↑ ↑ ↑ [22] |
|||
Neurogenesis | ↓ brain tissue postmortem (hippocampus) [23] |
↓Proliferation and differentiation of neural progenitor cells in APP/PS1 and 3xTg-AD mouse models [24,25] | ||
Calmodulin | ↓ brain tissue postmortem [26] |
|||
Primary cilia | ↓ in dentate gyrus cells of 3xTg-AD mice [27] ↑ in length in hippocampus of APP/PS1 mice [28] |
|||
Acetylcholine | ↓ [29] |
This Table summarizes the findings regarding the most accepted and widely described biomarkers, such as amyloid-β and tau proteins in blood and cerebrospinal fluid (CSF), postmortem human brains, and PET images. In addition, in biological processes altered in Alzheimer’s disease, molecules such as calmodulin and organelles as primary cilia are shown as sources of potential biomarkers in different human fluids and tissues, as well as in transgenic animal models of AD. ↑: increased; ↓: decreased; *: in blood exosomes.